General anaesthesia for major trauma
Background
Trauma is a pathology that is common and is associated with significant mortality and long-term morbidity in survivors. Management of the patient with multiple injuries requires the teamwork of several medical and surgical specialties. Injuries must be prioritized and dealt with in a timely manner. The anaesthetist will be involved in managing trauma patients throughout the patient’s journey and has a central role not just in anaesthetizing for surgical procedures, but also in optimizing the conditions that will improve the likelihood of survival and recovery.
Learning outcomes
1 Understand the role of the anaesthetist in reducing trauma-related mortality
2 Understand the need to prioritize management of injuries in a polytrauma patient
3 Consider the global picture of organ support when anesthetizing the polytrauma patient
4 Understand how trauma can impact upon the conduct of anaesthesia.
CPD matrix matches
2A02; 2C01
Case history
You are the on-call anaesthetist called to the ED, as part of the trauma team. A 35-year-old motorcyclist was involved in a collision with a car. The paramedics hand over to the ED team leader whist the gentleman is being assessed by the emergency medicine registrar, establishing that the gentleman has:
◆ An absence of C-spine symptoms: triple C-spine immobilization and a spinal board are in situ
◆ A patent airway with no signs of obstruction
◆ RR of 24/min, SpO2 95% on high-flow oxygen through a ‘trauma mask.’ Chest examination reveals pain on the left side of the chest
◆ HR 110 bpm, BP 95/55 mmHg, CRT 3 s, cool hands. An IV cannula is inserted, venous blood drawn, and 500 mL of warmed Hartmann’s solution administered, resulting in the HR falling to 100 bpm and an increase in BP to 100/60 mmHg
◆ His eyes are open, and he obeys commands, but his speech is confused. His pupils are equally reactive to light. Witnesses reported that he was initially unconscious but spontaneously recovered before the ambulance arrived. His blood sugar is 6.0 mmol/l.
◆ His temperature is 36.1°C. His abdomen is tender and guarded, and he has an obviously deformed, painful right thigh.
Why is the anaesthetist crucial for the management of a trauma patient?
There are approximately 5 million trauma deaths per year worldwide. In western countries, trauma is the fourth leading cause of death, and the incidence is highest in younger patients. In addition, for every trauma death, there are two survivors with long-term health issues. Worldwide, traumatic injuries account for 12% of the world’s health burden. The ultimate aims of trauma care are to:
1 Reduce the likelihood of early death
2 Prevent complications that cause late deaths and impair the quality of life in survivors.
Deaths in trauma occur in a trimodal distribution over time, according to the pathology involved (see Figure 2.8).
Fig. 2.8 The trimodal distribution of death following major trauma. From Trunkey DD. Trauma Sci Am 1983; 249(2): 20–7.
Peak 1 represents death occurring seconds to minutes following trauma and generally involves severe injuries of the airway, myocardium, great vessels, or brain. It is unlikely that medical care, however prompt, could prevent these deaths.
Peak 2 is accounted by deaths occurring minutes to hours following trauma. Injuries may be in the thorax, abdomen, cranium, or skeleton and are usually associated with haemorrhage. To improve the likelihood of survival, these patients require rapid assessment to identify injuries, with simultaneous resuscitation, followed by early intervention to correct the injuries, which may consist of surgery or IR.
The third ‘peak’ of deaths occurs days to weeks following trauma, even after definitive correction of the traumatic injuries has occurred. The pathology associated with these deaths includes sepsis and multiorgan failure. Aspects of care provided at all stages of the pathway will impact on the likelihood of infection or organ failure.
Trauma management is a core skill of the anaesthetist who may be involved in the care of the trauma patient at the following stages:
◆ Pre-hospital: advanced airway management and resuscitation
◆ ED: primary survey, airway management, ventilation, cardiovascular support, IV access, advanced monitoring, haemorrhage management
◆ Transfer: intrahospital transfer to radiology or theatre, or interhospital transfer to a tertiary care facility
◆ Intraoperative: provision of anaesthesia and organ support
◆ Post-operative: provision of organ support and re-establishment of homeostasis in level 2/HDU or level 3/ICU.
Case update
The patient remains tachypnoeic, and a CXR shows some left-sided rib fractures and left upper lobe opacification. He requires 500 mL of Hartmann’s solution to maintain a systolic BP above 80 mmHg. His bladder is catheterized.
An X-ray of his femur shows a displaced mid-shaft fracture. He has a femoral nerve block performed, and his leg is placed in a femoral traction device.
He is transferred to the radiology department where a full body CT scan is performed. Findings on CT scanning are:
◆ Right frontal lobe contusion with small subdural collection
◆ No evidence of C-spine injury
◆ Left-sided pulmonary contusions
◆ Small bowel thickening and extraluminal gas, suggesting disruption
◆ Right femoral mid-shaft fractures.
The orthopaedic surgeon is keen to proceed with nailing of the femoral fracture, and the general surgeon is keen to proceed with laparotomy. The neurosurgical opinion is that no operative intervention is required.
How should the treatment of these injuries be prioritized?
The trauma patient will often have multiple injuries that require input from different surgical specialties. A global view of the patient must be taken to avoid inappropriate or disordered surgical procedures. Interventions to deal with injuries must be both prioritized and timely to facilitate favourable patient outcome.
Prioritization of operative procedures can be achieved by considering:
◆ Which injuries will lead to death most quickly
◆ Which injuries must be addressed to allow stabilization
◆ Which injuries can be delayed until stabilization has occurred.
Table 2.4 outlines a model of triage for surgical correction when dealing with multiple injuries in polytrauma.
Table 2.4 Timing of surgical intervention
| Timing | Rationale | Examples |
|---|---|---|
|
Immediate |
Necessary to prevent early death Allows physiological stabilization |
Haemorrhage control: • Vascular repair Cavity decompression: • Craniotomy Cavity decontamination • Bowel repair |
|
Physiological correction |
||
|
Early (day 1) |
Can be delayed to allow physiological stabilization |
Fracture stabilization: • Femoral nailing Soft tissue debridement: • Burns debridement |
|
Late |
Reconstructive surgery |
Historically, it was recognized that trauma patients would experience a ‘second hit’ if they had operative management, i.e. a worsening of their clinical condition despite surgery. For this reason, penetrating abdominal trauma was managed expectantly until the first World War, and skeletal injuries were managed by immobilization until 1970s. This ‘second hit’ in now recognized as further activation of the neurohormonal stress response associated with oxidative dysfunction within the mitochondria.
Surgical management of the trauma patient has moved from ‘expectant/non-operative’ management, through a period of ‘early total care’ when all injuries would be corrected at an early stage. This approach saw unwell trauma patients exposed to insults that could have been delayed until they were physiologically stabilized.
Currently, all procedures that are necessary to sustain life and prevent early death are performed immediately. These are procedures without which stabilization cannot occur and include arresting of haemorrhage, decompression of the brain, and decontamination of cavities.
Case update
Following these procedures, the patient who has undergone multiple insults, and at risk of anaemia, coagulopathy, acidosis, hyperthermia, and other metabolic derangements, can have their physiology normalized in intensive care. When they have been stabilized, further necessary, but not life-threatening, procedures can be carried out. This approach is known as damage control.
The subject patient has two injuries requiring surgical attention. The fractured femur requires an intramedullary nail, and the small bowel injury necessitates a laparotomy. A fractured femur can be a life-threatening injury, as it can cause haemorrhagic shock, due to the associated blood loss. The bowel injury will cause soiling of the abdominal cavity and lead to septic shock, unless it is repaired. Of these injuries, addressing the fractured femur would be prioritized over the abdominal injury, according to the ‘ABCDE’ approach to triage. However, with the femur in traction and immobilized externally, the haemorrhage associated with the injury will be contained, and operative management can be delayed. This means the abdominal injury should be addressed immediately, and the general surgeons have priority to proceed.
What are the issues when considering anaesthetizing this patient?
◆ Airway and C-spine management:
• The patient is unfasted and at risk of aspiration of gastric contents
• The C-spine cannot be clinically ‘cleared’, and so CT radiological evidence of injury must be absent before removing the collar–blocks–tape immobilizing devices. Intubation will require manual in-line stabilization and may be difficult
◆ Respiratory:
• The patient will require PPV in the presence of a pulmonary injury
◆ Cardiovascular.
• The patient is at risk from hypovolaemia and sepsis. Optimizing oxygen delivery will be aided by attention to:
• Advanced monitoring: an arterial line will allow continuous BP measurement. Cardiac output monitoring (such as the Cardio-Q® oesophageal Doppler, LidCCO®, LidCCO Rapide®) is a non-invasive means for stroke volume variation, cardiac index, and systemic vascular resistance, which provide evidence of fluid filling status, contractility, and vascular tone, respectively
• Hb: the vehicle of oxygen carriage should be monitored, as there has been significant blood loss and clear fluid administration
• Coagulation: given the trauma, blood loss, and risk of sepsis, the patient is at risk of coagulopathy
• Lactic acidosis: an objective measure of cellular anaerobic metabolism is provided by monitoring pH/H+, BE, and lactate
◆ Neurological:
• The patient has a mild head injury, but this could worsen in the perioperative period. Attention should be paid to neuroprotective measures
◆ Renal:
• The patient has risk factors for developing an acute kidney injury. Intraoperative renal support should consist of optimizing perfusion of the kidneys by attaining an adequate MAP for renal perfusion, minimizing exposure to renal toxins, and monitoring urine output
◆ Hepatic:
• The shocked patient may develop a delayed hepatic dysfunction. Intraoperatively, hepatic perfusion of oxygenated blood at normal MAP will support hepatic function
◆ Metabolic:
• In addition to the acid–base disturbance, this patient may develop hypocalcaemia, hypomagnesaemia, hypokalaemia, and hypophosphataemia in the post-operative period
◆ Sepsis:
• The abdominal cavity is likely to be soiled and the immune function reduced by the stress response. Treatment-dose antibiotics covering intestinal aerobic and anaerobic organisms should be given, according to local protocols
◆ Temperature:
• There are risk factors for perioperative hypothermia. An indwelling temperature probe should be placed. Heating blankets and warmed IV fluids should be used to minimize heat loss
◆ Anaesthesia:
• Choices of drugs for induction, neuromuscular blockade, and maintenance will need to be rationalized and adjusted, given the risks of hypovolaemia, hypothermia, sepsis, and neurological injury
◆ Analgesia:
• Intraoperative analgesia will allow reduction of anaesthetic drug dosages and reduce the risk of developing chronic pain. Post-operative pain management should be planned. The risk and benefits of regional analgesia can be considered.
How should the airway be managed for this general anaesthetic? Are there any anticipated difficulties?
This patient should receive an RSI of general anaesthesia, with the placement of a cuffed ETT. The elements of RSI are pre-oxygenation, cricoid pressure on loss of consciousness, a tilting table, and the availability of suction. There are numerous risk factors for aspiration of gastric contents that can lead to physical obstruction of the airway or pneumonitis. The risk factors for aspiration present here are:
◆ Major trauma: sympathetic activity inhibiting gastric motility
◆ Opioid use
◆ ‘Unfasted’ status
◆ Intra-abdominal injury: producing gastric stasis
◆ Head injury: obtunding laryngeal reflexes.
As with any general anaesthetic, unanticipated difficult laryngoscopy may be encountered, and the strategy of airway management should be decided upon before induction of anaesthesia. In this case, since an RSI has been determined necessary, should the anaesthetist fail to intubate the trachea on three attempts, they should proceed with awakening the patient whilst maintaining oxygenation and ventilation.
How should general anaesthesia be induced and maintained?
The aims of induction are to:
◆ Rapidly achieve adequate anaesthesia and neuromuscular block
◆ Allow tracheal intubation
◆ Prevent aspiration of gastric contents
◆ Prevent hypoxia and cardiovascular instability.
As mentioned, this patient mandates an RSI. There are several drugs that could be used to achieve this end. The pharmacokinetics of the drugs and the patient’s condition should be considered when choosing agents.
Induction agents
◆ Thiopentone: this barbiturate is classically used in an RSI at 3–5 mg/kg. Thiopentone has the advantage of acting in one arm–brain circulation with a definitive endpoint, and it is a potent suppressor of seizure activity. However, in hypovolaemia, cardiac output is diverted to the vital organs such as the heart, lungs, and brain, and so proportionally more of the drug will be distributed to these organs. As a result, a smaller dose is required to induce anaesthesia, and hypotension secondary to reduced contractility and vasodilation will occur at smaller doses than in the normal patient. In addition, in the acidotic patient, a greater portion of the administered drug will be available in an unionized form and therefore have a more profound effect. Thus, in the presented case, thiopentone should be used cautiously and at a smaller dose. It is not possible to calculate an accurate dose reduction that will induce anaesthesia and yet avoid cardiovascular collapse
◆ Propofol: this phenol derivative has largely replaced thiopentone in routine anaesthetic practice at a dose of 2–3 mg/kg. Its endpoint is not as definite as thiopentone but will induce anaesthesia rapidly. In the shocked patient, cardiac output and drug distribution will be preferentially to the vital organs, and so smaller doses than normal will induce anaesthesia and cardiovascular compromise
◆ Etomidate: this imidazole derivative is useful, as it does not cause cardiac depression and vasodilation associated with thiopentone or propofol, when used in normal doses of 0.2 mg/kg. Thus, an accurate dose can be rapidly administered without impairing oxygen delivery. There are concerns regarding etomidate in that it temporarily inhibits the adrenal synthesis of glucocorticoids required to mediate the stress response. Infusion of the drug for sedation is associated with increased mortality in ICU patients; however, a single dose for induction has not been associated with worse outcome
◆ Ketamine: induction using this agent at 1–2 mg/kg is less rapid, yet it generally confers cardiovascular stability due to anticholinergic and sympathetic activity. It will temporarily increase the ICP and has traditionally been avoided in head-injured patients. However, the agent has neuroprotective properties, and the maintenance of cardiovascular stability and oxygen delivery may outweigh the transitory effect of increase in ICP
◆ Midazolam: this benzodiazepine is the slowest agent, if used singularly. Although it causes minimal cardiovascular disturbance, it is useful to supplement induction when used with thiopentone or propofol, as it allows dose reduction of the drugs associated with cardiovascular disturbance
◆ Opioids: used alone, these agents will not cause rapid loss of consciousness, but, as the effect of agents is additive, they are useful as co-induction agents and cause minimal cardiovascular disturbance. Fentanyl and alfentanil bolus dose before induction will allow dose reduction of thiopentone or propofol. Alternatively, infusion of remifentail can be used. The latter has the advantages that it can be infused according to body mass or titrated to the desired plasma or ‘effect’ site concentration, according to kinetic modelling infusion devices. In addition, opioids will obtund the sympathetic response to laryngoscopy, reducing surges in ICP.
Neuromuscular blockade
The choice of agent to achieve ‘paralysis’ to facilitate intubation and ventilation is between suxamethonium and rocuronium.
◆ Suxamethonium: this is an agent traditionally used in RSI at 1–2 mg/kg, as it provides intubating conditions in 45 s. As it will temporarily increase ICP, co-induction with opioids should be carried out. Other serious potential risks with suxamethonium are anaphylaxis and malignant hyperthermia. In addition, hyperkalaemia may occur in those with chronic neuromuscular conditions, as well as those with severe burns or immobility of >48 hours’ duration. Normally, a short-acting second agent is needed to maintain neuromuscular blockade. If pseudocholinesterase deficiency is present, a prolonged effect may occur
◆ Rocuronium: if used for RSI, a dose of 1 mg/kg will achieve intubating conditions in 60 s. Rocuronium is associated with a risk of anaphylaxis but is not associated with malignant hyperthermia or hyperkalaemia. Unlike suxmethonium, rocuronium is not a short-acting agent, and a dose of 1 mg/kg will provide up to an hour of effect.
Maintenance of anaesthesia in the trauma patient case can be achieved by inhalational of volatile anaesthetic or total intravenous anaesthesia (TIVA). Evidence to support one technique over another in a trauma patient is absent.
It should be remembered the trauma patient may be hypovalaemic. This is significant for two reasons:
1 The cardiovascular system will be attempting to compensate by tachycardia and vasoconstriction to maintain BP. Anaesthetic agents, with the exception of ketamine, will suppress the cardiovascular system, and a normal dose may cause decompensation and worsen tissue perfusion. Lighter doses of volatile (0.7–1.0 minimum alveolar concentration, MAC) or lower target-controlled infusion (TCI) of propofol (3.0–4.0 micrograms/mL) may be needed to avoid this
2 In shock, splanchnic, renal, skeletal, and skin perfusion is reduced; the cardiac output is diverted to the heart, lungs, and brain. Thus, proportionally more anaesthetic will be distributed to the brain and heart. This allows a reduced dose of the administered agent to achieve anaesthesia, and fortunately a reduction in the cardiovascular depression.
Methods to reduce the anaesthetic dose, whilst maintaining cardiovascular stability, include:
◆ Opioid administration
◆ Benzodiazepine administration
◆ Regional analgesia preoperatively: the femoral nerve block will reduce afferent pain stimulation of the cerebrum and reduce sedation requirement. Central neuroaxial blockade is a risk to the trauma patient who is hypovolaemic, as it may provoke cardiovascular collapse, and unrecognized coagulopathy may result is epidural haematoma.
Inappropriate methods in this patient due to the aim of neuroprotection are:
◆ Nitrous oxide: will increase cerebral oxygen consumption
◆ Ketamine infusion: will increase ICP.
Whichever technique is chosen, it should be noted that emergency/trauma anaesthesia has been associated with an increased risk of awareness. This is possibly because lighter doses of anaesthesia are used to avoid cardiovascular depression in the hypovolaemic–acidotic patient. In addition, the use of TIVA and continuous neuromuscular blockade have also been associated with increased risk of awareness. In patients with an increased risk of awareness, the bispectral index (BIS) can provide an indication of the depth of anaesthesia. This dimensionless number, derived from frontotemporal electroencephalograms (EEGs), indicates cortical activity, with 100 being normal and 0 being isoelectric. A BIS of 40–60 is associated with a low probability of conscious recall and can be used to titrate anaesthetic dose. It should be noted that there is considerable interindividual variability with BIS and conscious level, and there is conflicting evidence on the efficacy of BIS in reducing the risk of awareness.
What are the issues with ventilation of this patient?
The overall aim of cardiorespiratory support is cellular oxygenation to meet metabolic demands and avoidance of anaerobic metabolism and acidosis. Intraoperative ventilation should be aimed at:
◆ An adequate PaO2 that achieves saturation of Hb
◆ Low to normal PaCO2
◆ Minimizing the risk of ventilator-induced lung injury (VILI).
The role of the respiratory system is to develop a partial pressure of oxygen in the pulmonary capillaries that will saturate the Hb molecules within erythrocytes, thus optimizing arterial oxygen content. An inadequate partial pressure of oxygen in capillary blood will reduce the percentage of Hb that is saturated with oxygen, risking inadequate arterial oxygen content and subsequent lactic acidosis. Appropriate monitoring of the respiratory system of this patient intraoperatively consists of continuous pulse oximetry and intermittent arterial blood analysis of PaO2. Monitoring of pulmonary capillary blood is not possible, but arterial PaO2 is the best surrogate indicator.
The ventilator parameters that can be adjusted to improve PaO2 are:
◆ Minute ventilation (MV): the product of tidal volume (Vt) and RR. Tidal volume can either be controlled directly (volume-controlled ventilation) or indirectly by varying the inspiratory pressure (pressure-controlled ventilation)
◆ FiO2
◆ PEEP: general anaesthesia, supine position, and alveolar pathology will predispose to alveolar collapse which can be overcome by PEEP. Studies in ALI in intensive care patients have shown no adverse outcome when comparing higher levels of PEEP to lower levels.
The ventilator parameters of inspiratory pressure, tidal volume, PEEP, RR, and FiO2 can be adjusted to achieve appropriate oxygenation.
The other role of the respiratory system is the excretion of carbon dioxide. This product of aerobic metabolism is a volatile acid. Hypercarbia contributes to cellular acidosis and will cause an increase in cerebral blood volume by cerebrovasodilation, risking a rise in ICP in head injury. Conversely, hypocarbia (PaCO2 <4.0 kPa) will cause cerebrovasoconstriction and impair oxygen delivery in the brain. For these reasons, it is considered neuroprotective to target a PaCO2 of 4.0–4.5 kPa. There is an inverse linear relationship between alveolar PCO2 and MV; so, in order to reduce PaCO2, MV must be increased.
PPV is a means to achieve oxygenation and normocarbia, but it is not without risk. The physical forces involved in PPV induce inflammatory changes within the lung, known as VILI. In patients with ALI, a lung-protective ventilation strategy of restricting the tidal volume to 6 mL/kg (ideal bodyweight) and the inspiratory plateau pressure to 30 cmH2O is associated with a reduction in mortality. The inflammatory changes associated with PPV are known to occur early in the ventilation period in normal lungs, not as a late consequence. Given the presence of the pulmonary contusions and the possibility of post-operative ventilation, lung-protective ventilation is a strategy that may reduce the likelihood of post-operative respiratory complications.
The process of cellular oxygen utilization to produce adenosine triphosphate (ATP) involves several enzyme-dependent steps during the citric acid cycle and the electron transport chain. Under conditions of stress, including trauma, the utilization of oxygen can become dysfunctional and lead to the incomplete reduction of oxygen to water, generating charged free radical species that cause irreversible mitochondrial damage. High levels of oxygen supplied to the dysfunctional cell will fuel the formation of these free radicals, and so the lowest FiO2 consistent with an adequate Hb saturation should be used.
What influence does a head injury have on the management of a trauma patient?
Although this patient does not require neurosurgery, he nonetheless has a significant primary brain injury. The principle in management of this injury is the prevention of secondary brain injury throughout the perioperative period. This is achieved by ensuring cerebral oxygenation and prevention of a rise in ICP. The following factors should be addressed to achieve this end:
◆ Airway: laryngoscopy and the presence of an ETT will evoke a sympathetic response, increasing the cerebral blood volume and pressure, as will coughing or straining. These responses can be reduced by adequate doses of anaesthetic and opioids, and the maintenance of neuromuscular blockade. In addition, the ETT should be secured with tape, not a tie which can reduce jugular venous drainage
◆ Gas exchange: hypoxia and hypercarbia will cause cerebral vasodilation and an increase in ICP. The patient should be ventilated to achieve a PaO2 >10 kPa and PaCO2 4–4.5 kPa. PEEP should be minimized to prevent elevation in jugular venous pressure (JVP)
◆ CPP is required to perfuse the brain (CPP = MAP – ICP). Normally, CPP is constant over a range of MAP, from 50 to 150 mmHg, because of autoregulation, i.e. cerebrovasodilation in response to hypotension and cerebrovasoconstriction in response to hypertension. In brain injury and under anaesthesia, autoregulation is obtunded, and so perfusion becomes dependent on the MAP. For this reason, normotension should be targeted and hypotensive resuscitation avoided
◆ Hb concentration
◆ Anaesthesia: volatile agents will reduce the cerebral demand for oxygen, protecting against hypoxia. However, it will also cause dose-dependent cerebrovasodilation, which increases ICP. On balance, a MAC of 0.7–1.0 should allow adequate anaesthesia, without raising ICP. Opioids will supplement anaesthesia, in addition to analgesia, obtunding laryngeal reflexes, e.g. remifentanil infusion. Ketamine has traditionally been associated with increasing ICP.
Case update
The general surgeons perform a laparotomy and find two full-thickness disruptions of the jejenum. They perform two short resections and end-to-end anastomoses of the small bowel and lavage the abdominal cavity. No other injuries are found, and the abdomen is closed within an hour of beginning the procedure.
The patient remains stable throughout the procedure.
Table 2.5 shows the results of the intraoperative arterial and venous blood analysis performed intraoperatively.
Table 2.5 Intraoperative arterial and venous blood results
| Parameter (normal range) | Result |
|---|---|
|
H+ (35–45 nmol/L) |
44 |
|
HCO3– (22–28 mmol/L) |
21 |
|
Lactate (0.0–2.0 mmol/L) |
2.0 |
|
BE (–2.0 to 2.0) |
2.0 |
|
PaO2 (11–13 kPa) |
11 (FiO2 0.4) |
|
PaCO2 (4.0–6.0 kPa) |
4.5 |
|
Hb (12–17 g/dL) |
9.0 |
|
WCC (4.0–9.0 x 109/L) |
5.0 |
|
Plt (150–400 x 109/L) |
200 |
|
PT ratio (1.0) |
1.2 |
|
APTT ratio (1.0) |
1.2 |
|
Fibrinogen (1.5–3.5 g/dL) |
2.0 |
Given the patient’s stability and lack of metabolic derangement, it is decided to proceed with the insertion of an intramedullary nail to the fractured femur. General anaesthesia is continued for this procedure, during which the patient loses approximately 750 mL of blood and requires 1 L of Hartmann’s solution. The procedure takes 90 min. Towards the end of the procedure, a near-patient HemoCue® shows a Hb of 7.0 g/dL. An ABG shows H+ 50 nmol/L, BE –4.0 mmol/L, and lactate 3.0 mmol/L.
Should this patient be extubated following the surgical procedure, or should ventilation continue in the post-immediate post-operative period?
The advantage of extubation following surgery is that the patient is no longer exposed to the risks of PPV, i.e. physical forces that induce inflammation and dysfunction of the respiratory membrane, known as VILI. Ventilation is also associated with barotrauma, wasting of the respiratory muscles, VAP, impairment of haemodynamics, and inflammatory changes in distant organs.
To minimize the risks of mechanical ventilation, patients should be extubated and returned to spontaneous negative pressure ventilation as soon as it is likely they will not develop respiratory failure post-extubation.
Patients at risk of respiratory failure should be identified before extubation. The Difficult Airway Society has produced an extubation guideline (see Figure 2.9) to assist with stratifying patients into low-risk or high-risk groups for adverse events post-extubation and forming a strategy for managing the high-risk group.
Fig. 2.9 Difficult Airway Society extubation guideline. Reproduced with permission from V. Mitchell et al., ‘Difficult Airway Society Guidelines for the management of tracheal extubation’, Anaesthesia, 67, 3, pp. 318–340, © 2012 The Association of Anaesthetists of Great Britain and Ireland.
Extubation is a high-risk stage in the perioperative period that can lead to complications. In our subject case, the most likely complications following extubation are aspiration and respiratory failure. The general risk factors for respiratory failure are:
◆ Cardiovascular:
• The patient has undergone a major trauma followed by two surgical procedures of intermediate risk. Each of these contributes to the stress response, increasing oxygen demand and placing demands on the cardiovascular system to increase oxygen delivery. The stress response is known to continue for 48 hours following a major surgery. Continued sedation and ventilation in the immediate post-operative period will reduce oxygen consumption
◆ Respiratory:
• The patient has pulmonary contusions that are at risk of worsening during the intraoperative period. An assessment of the function of the respiratory membrane can be made by comparing the partial pressure of oxygen of arterial blood to that of inspired gas (P/F ratio)
◆ Neurological:
• Brain injury: the patient’s preoperative mild brain injury may have worsened despite neuroprotective measures. On emergence from anaesthesia, this may manifest as acute confusion, causing ineffective ventilation
• Pain: untreated pain is a risk factor for post-operative respiratory failure. Similarly, excessive use of opioid may cause hypoventilation
◆ Metabolic:
• Metabolic acidosis creates an oxygen debt for which the respiratory system will try to compensate. On emergence from anaesthesia, this may cause a rapid, inefficient ventilation and respiratory failure
• Disturbance of calcium and magnesium homeostasis may result in inefficient respiratory muscle activity
• Hypothermia: the expenditure of energy in shivering and cerebral dysfunction in the hypothermic patient may contribute to post-operative respiratory failure.
Case update
It is decided that the patient should be kept sedated and ventilated, and admission to the ICU is organized.
Over the next 12 hours, he is ventilated with a lung-protective strategy; he has his Hb kept above 8.0 g/dL with red cell transfusion, and his BE returns to normal. His PaO2 is kept above 10 kPa with an FiO2 of 0.3, PEEP of 5 cmH2O, and the inspiratory support is weaned. He is extubated and maintains an SpO2 of 95% on FiO2 of 0.4, with no signs of respiratory distress. Serial CXRs show a gradual resolution of the pulmonary contusion.
The patient resumes oral intake of nutrition and is discharged to the orthopaedic ward on day 2 post-operatively.
Summary
Trauma is a common pathology that is associated with significant mortality and morbidity in survivors. Those surviving the initial injury are at risk of dying early due to their injuries, or dying later as a result of multiorgan dysfunction and sepsis. Following an initial assessment and resuscitation measures, potential injuries should be suspected. If the patient is stable, a whole body imaging will allow diagnosis and the prioritized management of underlying injuries. Cardiovascular instability is an indication for surgery directed at haemorrhage control before diagnosing and managing other injuries. The anaesthetist should aim to maintain adequate cellular oxygenation to limit anaerobic metabolism and acidosis, to support other organ systems, and to minimize the potential for sepsis. A multisystem model of care will allow the support of vital organs. Anaesthesia should be conducted, respective of the patient’s past medical history and their acute injuries and physiological status. All supportive therapies, from oxygen administration to ventilation, inotropic/vasopressor support, and renal replacement therapy (RRT), carry an inherent risk of iatrogenic injury and should be de-escalated, when appropriate, to minimize this risk.
American College of Surgeons Committee on Trauma (2008). ATLS Student Course Manual, 8th edn. American College of Surgeons, Chicago (ISBN 978–1–880696–31–6).
Difficult Airway Society. DAS extubation guidelines. Available at: <http://www.das.uk.com/content/das-extubation-guidelines>.
Kilpatrick B and Slinger P (2010). Lung protective strategies in anaesthesia. British Journal of Anaesthesia, 105 (suppl 1), 108–16.
National Confidential Enquiry into Patient Outcome and Death (2007). Trauma:who cares? Available at: <http://www.ncepod.org.uk>.
Nicola R (2013). Early total care versus damage control: current concepts in the orthopedic care of polytrauma patients. ISRN Orthopedics, 2013, article ID 329452.
Patel P (2005). An update on neuroanesthesia for the occasional neuroanesthesiologist. Canadian Journal of Anesthesia, 52, 6.